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Peter H. Duesberg1,*, Daniele Mandrioli1, Amanda McCormack1, Joshua M. Nicholson2, David Rasnick3, Christian Fiala4, Claus Koehnlein5, Henry H. Bauer2 and Marco Ruggiero6
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IJAE Vo l.116,n.2: 73-92, 2011
ITALIAN JOURNAL OF ANATOMY AND EMBRYOLOGY
Submitted February 14, 2011; accepted June 16, 2011
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Author
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Peter Duesberg
Daniele Mandrioli
Amanda McCormack
Joshua M. Nicholson
David Rasnick
Christian Fiala
Henry Bauer
Marco Ruggiero
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Publisher
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IJAE
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Topic
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Publish Year
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2011
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Content Type
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Scientific Paper
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Description
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Summary
Since the discoveries of a putative AIDS virus in 1984 and of millions of asymptomatic carriers in subsequent years, no general AIDS epidemic has occurred by 2011. In 2008, however, it has been proposed that between 2000 and 2005 the new AIDS virus, now called HIV, had killed 1.8 million South Africans at a steady rate of 300,000 per year and that anti-HIV drugs could have saved 330,000 of those. Here we investigate these claims in view of the paradoxes that HIV would cause a general epidemic in Africa but not in other continents, and a steady rather than a classical bell-shaped epidemic like all other new pathogenic viruses. Surprisingly, we found that South Africa attributed only about 10,000 deaths per year to HIV between 2000 and 2005 and that the South African population had increased by 3 million between 2000 and 2005 at a steady rate of 500,000 per year. This gain was part of a monotonic growth trajectory spanning from 29 million in 1980 to 49 million in 2008. During the same time Uganda increased from 12 to 31 million, and Sub-Saharan Africa as a whole doubled from 400 to 800 million, despite high prevalence HIV. We deduce from this demographic evidence that HIV is not a new killer virus. Based on a review of the known toxicities of antiretroviral drugs we like to draw the attention babies and all others who carry antibodies against HIV.
Key words
HIV; population growth; anti-HIV agents; AIDS drugs; drug toxicity.
1. Introduction
In 1984 the hypothesis was advanced in the US that a new AIDS virus was at the classic germ theory of disease (Gallo et al., 1984; Altman L.K., newspaper arti cle in the New York Times, New York, pp. C1-C3, April 24, 1984). This virus-AIDS hypothesis has since monopolized AIDS research and the treatment and prevention of AIDS, although the predicted general epidemic never showed up. In view of this we have re-analyzed the epidemiology of AIDS and HIV, particularly of Africa, which made by the classic germ theory of disease.
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This issue is of interest also for embryologists, who are called to evaluate the potential and actual effects of antiretroviral drugs on developing humans during prenatal life and in babyhood.
2. Population of South Africa grows steadily, despite claims of huge losses from a new epidemic of HIV
To answer our question about the reportedly huge losses of South African lives from HIV, we checked three sources:
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3) Population statistics of South Africa. In an effort to obtain further independent evidence for HIV-dependent life losses, we looked for a corresponding decline in the population growth trajectory of South Africa. Unexpectedly we found that the population of South Africa had increased by 3 million from 2000 to 2005, based on concordant statistics from South Africa and the US Census Bureau (Statistics South Africa, 2007; US Census Bureau, International Data Base, 2008). As shown in Tab. 1 and Fig.
4A, this gain extended a steady growth trajectory of South Africa from 29 million in 1980 to 47.5 million in 2005, which then continued at the same steady rate (Statistics South Africa, 2000; Statistics South Africa 2007; US Census Bureau, International Data Base, 2008). The change of the growth trajectory predicted by the losses of 300,000 per year for 6 years is shown as a hypothetical branch of the observed monotonic growth curve in Fig. 3A. But the actual growth curve did not show any evidence for such loss-
es. In sum, the South African population grew steadily during the period from 2000-2005, extending a long-established growth trajectory. Indeed, this growth curve has been so consistently monotonic that it predicted exactly the increase of the South African population by 3 million between 2000 and 2005 (see Tab. 1, Fig. 4A).
Table 1 – Population statistics of South Africa from 1980 until 2008.
Year Population | HIV+ | HIV-Death | |
x10-3 (a) | % (b) | x10-3 (c) | |
1980 | 29,300 | ||
1981 | 30,200 | ||
1982 | 31,100 | ||
1983 | 32,100 | ||
1984 | 33,200 | ||
1985 | 34,300 | ||
1986 | 35,100 | ||
1987 | 35,900 | ||
1988 | 36,800 | ||
1989 | 37,600 | ||
1990 | 38,500 | 0.7 | |
1991 | 39,300 | 1.7 | |
1992 | 40,100 | 2.2 | |
1993 | 40,900 | 4.0 | |
1994 | 41,600 | 7.6 | |
1995 | 42,200 | 10.4 | |
1996 | 42,800 | 14.4 | |
1997 | 43,300 | 17.0 | * |
1998 | 43,900 | 22.8 | * |
1999 | 44,500 | 22.4 | 10.0 |
2000 | 45,100 | 24.5 | 10.5 |
2001 | 45,600 | 24.8 | * |
2002 | 46,100 | 26.5 | * |
2003 | 46,600 | 27.9 | * |
2004 | 47,000 | 29.5 | 13.0 |
2005 | 47,500 | 30.2 | 14.5 |
2006 | 47,900 | 29.1 | |
2007 | 48,400 | 28.0 | |
2008 | 48,800 | ||
(a)Statistics South Africa and US Census Bureau (Statistics South Africa, 2007; Statistics South Africa, 2000; US Census Bureau, International Data Base, 2008).
(b)National Department of Health South Africa (National Department of Health South Africa, 2007).
(c) Statistics South Africa (Statistics South Africa, 2007; Statistics South Africa, 2008) Statistics South Africa. Mor- tality and causes of death in South Africa, 2006: Findings from death notification. Statistics South Africa, 2008.
*Not reported because HIV-deaths were below 10th rank.
Moreover, a new viral epidemic causing steady losses of 300,000 per year for 6 years is not compatible with the classic germ theory of disease. Instead, the germ theory predicts that new viruses and microbes cause epidemics that rise exponentially, because of exponential growth and spread of microbes, and then fall exponentially, because of the resulting immunity and deaths within several months, rather than go steady over 6 years (see Fig. 1 and Introduction). HIV has been demonstrated 20 years
ago to induce anti-viral immunity - but not AIDS - within several weeks after infection (Clark et al, 1991; Daar et al, 1991), just like any other virus (Duesberg, 1989). Thus a new virus could have been a plausible explanation for a seasonal epidemic of several months within a given year, but not for a steady loss of lives for 6 years in a row.
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To test our hypothesis that HIV may not be pathogenic, we asked next, whether the population growths of other HIV antibody-positive African countries were also independent of HIV, as for example Uganda.
3. Population of Uganda doubles despite HIV epidemic
Based on the AIDS literature, Uganda is the epicenter of the African AIDS epidemic and thus a primary challenge of hypotheses on the pathogenicity of HIV. In 1989 the Minister of Health has already announced that 5.8% of the population was HIV antibody-positive (Goodgame, 1990). It is for this reason that the New England Journal of Medicine described Uganda as a model for emerging AIDS epidemics in Africa: “AIDS is already the most common cause of admission and death among hospitalized adults” (Goodgame, 1990). Concordantly Mulder et al. claimed in 1994 in The Lancet and in Aids that, “Among adults, half of all deaths and among those aged 13-44 over 80% of deaths were attributable to HIV-1 infection” (Mulder et al., 1994a,b)
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The fact that the population of Uganda increased 2.5-fold during the HIV-AIDS era, although it was described in the professional literature as model for the dire con- sequences of a fatal HIV epidemic, lends support to our conclusion that South Afri- can population growth is also independent of HIV.
4. Population of total Sub-Saharan Africa doubles from 400 to 800 million between 1980 and 2007
In an effort to raise our investigation above variations among population statistics and AIDS epidemics of different African countries, we asked next whether the population of Sub-Saharan Africa as a whole was increasing or decreasing - in the face of the widespread prevalence of antibodies against HIV (Quinn et al., 1986; Goodgame, 1990; Merson, 1993; Mulder et al., 1994b; The Durban Declaration, 2000; Gisselquist et al., 2002).
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We conclude that the predicted epidemiological patterns associated with a widespread new killing virus never showed up in Africa. In the following we briefly investigate the theory that HIV is a passenger virus.
5. Could HIV be a passenger virus?
By definition a passenger virus is not sufficient and not necessary to cause a disease (Duesberg, 1994). A passenger virus can thus be associated with healthy people and also with people suffering from virus-independent disease. Human examples are cytomegalovirus, adenovirus or reovirus (Fenner et al., 1974; Fields, 2001).
The hypothesis that HIV is a passenger predicts that its spread and prevalence do not coincide with mortality. To test this prediction we investigated the effect of the spread and prevalence of HIV on the population growth curve of South Africa.
Table 2 – Population statistics of Uganda from 1980 to 2008.
Year | Population x 10-3 (a) |
1980 | 12,400 |
1981 | 12,700 |
1982 | 13,100 |
1983 | 13,500 |
1984 | 13,900 |
1985 | 14,400 |
1986 | 14,900 |
1987 | 15,600 |
1988 | 16,200 |
1989 | 16,800 |
1990 | 17,500 |
1991 | 18,100 |
1992 | 18,700 |
1993 | 19,400 |
1994 | 20,100 |
1995 | 20,700 |
1996 | 21,200 |
1997 | 21,900 |
1998 | 22,500 |
1999 | 23,200 |
2000 | 24,000 |
2001 | 24,700 |
2002 | 25,500 |
2003 | 26,300 |
2004 | 27,200 |
2005 | 28,200 |
2006 | 29,200 |
2007 | 30,300 |
2008 | 31,400 |
a) US Census Bureau (US Census Bureau, International Data Base, 2008).
For this purpose we plotted the HIV-antibody prevalence of the South African popula- tion reported by the National Department of Health South Africa since 1990 (Department of Health South Africa, 2007) on a separate panel of Fig. 4, which shows the population growth curve of South Africa. Fig. 4B shows that anti-HIV antibodies were first detected in 1990 in 0.7% of the population. This percentage then increased gradually (not exponentially!) over about 10 years until 2000, when it leveled off between 25 and 30%.
...
Likewise the CDC reports a steady 1 to 1.5 million of HIV-positive Americans since 1985 (see pages 186 and 191 above, and Duesberg et al. 2003). Since immigration of HIV-positives is banned, this indicates that the mortality of average American HIV-positives is close to normal. Furthermore, a study of the US Army reported recently that about 5% HIV-positive soldiers (Renzullo et al., 2001) “through an experiment of nature” developed no AIDS for up to 20 HIV-antibody-positive years without anti-HIV treatments (Okulicz et al. 2009), confirming the view that HIV is not sufficient for AIDS. The reason for AIDS-free HIV infection was not solved by the Army’s study. But since the Army’s study did not investigate the use of recreational drugs, although the majority of American AIDS patients have used recreational and anti-viral drugs (Duesberg et al., 2003, see also Introduction), it is possible that the AIDS-free HIV-positives were those who had used neither recreational nor anti-viral drugs. The toxic effects of antiviral drugs are described in the next section. Thus the CDC, the WHO and the US Army provide evidence that supports our demographic evidence that HIV is a passenger virus.
6. Can anti-HIV drugs be beneficial, particularly if HIV is not pathogenic per se?
The evidence that HIV may be not pathogenic casts a new light on the question how AIDS should be treated. In view of this we review here briefly the theoretical limits of anti-retroviral (anti-HIV) treatments, and then the effects of currently used anti-HIV drugs, particularly those recommended for South Africa (Chigwedere et al., 2008).
...
We deduce from these findings that anti-HIV drugs are inevitably toxic, can induce AIDS-defining and non-AIDS-defining diseases. We do not rule out, however, that anti-HIV drugs, owing to their inherent cytotoxic effects, can have beneficial effects against “opportunistic” microbial diseases and cancers, if prescribed for limited periods of time (Duesberg et al., 2003; Monini et al., 2004). In agreement with us a recent study in Nature Genetics warned about the “irreversible long-term effects of the drugs”, which “raise the specter of progressive iatrogenic mitochondrial genetic disease emerging over the next decade” (Payne et al., 2011). Other voices have also called for caution on when and how to start treatments of asymptomatic HIV-posi- tive subjects, which might enlarge the reader’s perspective on this point (DART Trial Team 2010; Sturt et al., 2010; Nunes et al., 2011; Panel de expertos de Gesida y Plan Nacional sobre el Sida, 2011; Siegfried et al., 2011).
7. General Conclusions
In sum, our analyses of African HIV- and AIDS prevalence revealed unexpected discrepancies between the reported epidemics of AIDS and of HIV. The predicted epidemiological pattern of mortality associated with the putative new AIDS virus never showed up in South Africa or anywhere else in Africa between 2000 and 2005. On the contrary, the African population doubled during the HIV-AIDS era, despite high prevalence of HIV. Our findings that there is no evidence for a new fatal HIV-AIDS epidemic in Africa have thus resolved the paradox that HIV would cause a general AIDS epidemic in Africa, but not in the rest of the world – namely by the absence of said epidemic.
In view of this and the inherent toxicities of anti-HIV drugs reviewed by us here, we propose a reevaluation of the HIV-AIDS hypothesis and of the prescription of anti-viral drugs to HIV antibody-positive subjects. Until there is verifiable evidence that HIV is fatally pathogenic, we deduce that South Africa’s ‘‘failure to accept the use of available ARVs [anti-HIV drugs]” (Chigwedere et al., 2008) has probably saved rather than cost South African lives.
Acknowledgments
We thank professors Ignacio Chapela (UC Berkeley), Bruce Charlton (Newcas- tle University, UK) and Eileen Gambrill (UC Berkeley) for critical and constructive reviews of this manuscript. Further we are indebted to Robert Hoffman (UC San Diego), Hans Kugler (Los Angeles), Kary Mullis (Newport Beach, California), Vidya Nanjundiah (Bangalore, India), Sigrid Duesberg (Berkeley), Bob Leppo (philanthropist, San Francisco), Jerry Pollack (Seattle, University of Washington) and Rudolf Werner (University of Miami, School of Medicine) for helpful comments and questions. We are grateful to Colonel Frank Anders, Lieutenant Colonel Clinton Murray and Major Jason Okulicz for encouragement, critical comments and for preliminary results on “HIV-Elite Controllers” (HIV-positives) from the US Military. In addition we gratefully acknowledge the Abraham J. and Phyllis Katz Foundation (Newnan, GA), an anonymous donor from Connecticut, Robert Leppo, Peter Rozsa (philanthropist, Los Angeles) and other private sources for support.
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AIDS since 1984: No evidence for a new, viral epidemic – not even in Africa
Note added in proof
After this manuscript went to press, Apostolova, Blas-Garcia and Esplugues have reviewed "the long-term adverse effects" of anti-HIV drugs including those of the non-nucleoside reverse transcriptase inhibitors such as Nevirapine. They found that these drugs cause "rash and hypersensibility reactions, hepatotoxicity, metabolic dis- turbances including lipodystrophy, pancreatitis, gastrointestinal toxicity, hyperlac- tatemia, hyperlipedimia, insulin resistance, and neuropsychiatric symptoms” (Blas- Garcia et al., 2011; Apostolova et al., 2011). These new findings confirm and extend reservations we have made here on similar grounds. Further we draw the attention of the reader to "The Myth of Heterosexual AIDS" by Fumento as independent evi- dence for the absence of a general AIDS epidemic in the US (Fumento, M, 1990).
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